Abstract
In individuals with advanced chronic kidney disease, secondary hyperparathyroidism is known to be associated with high turnover bone disease. Low serum parathyroid hormone (PTH) levels may not necessarily be because of hypodynamic bone, but could be another facet of the malnutrition-inflammation-cachexia syndrome (MICS). A recent 5-year cohort study in 748 stable hemodialysis outpatients showed that after the confounding effect by the MICS was removed, the moderately low levels of PTH in the 100 to 150 pg/mL range was associated with the greatest survival rate. Data from Japanese dialysis patients show similar survival advantages of having a lower PTH range. Low levels of serum PTH seem to be associated with markers of protein-energy wasting and inflammation, and this association may confound the relationship between serum PTH and alkaline phosphatase. PTH stimulates lipogenesis through influx of calcium into the adipocytes. PTH secretion is suppressed by interleukin-1 beta and interleukin-6, which are proinflammatory cytokines that are associated with poor outcome in dialysis patients. These cytokines inhibits PTH secretion in cultured parathyroid tissue slices. In this article, we review the association of a low serum PTH level with the MICS in patients with chronic kidney disease and suggest avoiding over-interpretation of low serum PTH level as an indicator of low turnover bone disease.
Highlights
In individuals who have chronic kidney disease (CKD), secondary hyperparathyroidism is associated with high-turnover bone disease, high fracture rates and higher death rates.[1,2] In dialysis patients, a serum parathyroid hormone (PTH) between 150 to 300 pg/ml is considered a reasonable target zone.[3]
The Kidney Disease Outcome Quality Initiative (KDOQI) and Kidney Disease Initiative Global Outcomes (KDIGO) guidelines suggest that serum PTH should be maintained above 150 pg/ml or 130 pg/ml, respectively, in chronic dialysis patients in order to avoid adynamic bone disease, while the Japanese Society of Dialysis Therapy (JSDT) recommends a target PTH range between 60 and 180 pg/ml.[4]
In the foregoing study, the inhibitory effect of IL-1β could be counteracted by the IL-1 receptor antagonist (IL-1ra),[12] indicating that the inflammation induced suppression of PTH can potentially be overcome by treatment of malnutrition-inflammation complex in individuals with CKD
Summary
In individuals who have chronic kidney disease (CKD), secondary hyperparathyroidism (serum PTH >65 pg/ml) is associated with high-turnover bone disease, high fracture rates and higher death rates.[1,2] In dialysis patients, a serum PTH between 150 to 300 pg/ml is considered a reasonable target zone.[3].
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